Anaphylaxis: A Practical Guide PDF
Preview Anaphylaxis: A Practical Guide
Anaphylaxis A Practical Guide Anne K. Ellis Editor 123 Anaphylaxis Anne K. Ellis Editor Anaphylaxis A Practical Guide Editor Anne K. Ellis Queen’s University Kingston ON Canada ISBN 978-3-030-43204-1 ISBN 978-3-030-43205-8 (eBook) https://doi.org/10.1007/978-3-030-43205-8 © Springer Nature Switzerland AG 2020 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recita- tion, broadcasting, reproduction on microfilms or in any other physical way, and transmission or infor- mation storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. 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This Springer imprint is published by the registered company Springer Nature Switzerland AG The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland Contents 1 Introduction to Anaphylaxis Essentials . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Shannon French and Anne K. Ellis 2 Early Recognition of Anaphylaxis in High Risk Settings . . . . . . . . . . . 11 David R. Stukus 3 Management of Anaphylaxis Refractory to Standard First Line Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 Catherine Hammond and Jay Lieberman 4 Biphasic Anaphylaxis: Epidemiology, Predictors, and Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Waleed Alqurashi 5 Exercise-Induced Anaphylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61 Babak Aberumand and Anne K. Ellis 6 In-Office Preparedness for Anaphylaxis . . . . . . . . . . . . . . . . . . . . . . . . . 69 Erin Banta and Marcella Aquino 7 Masqueraders of Anaphylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85 Julia E. M. Upton 8 Anaphylaxis Education: For Patients, Daycares, Schools, and Colleges . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 101 Nicole B. Ramsey and Julie Wang 9 Advocacy for Anaphylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115 Tonya Winders and Stanley Fineman 10 Resources for Anaphylaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123 Anne K. Ellis Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 v Contributors Waleed Alqurashi Division of Emergency Medicine, Department of Pediatrics, University of Ottawa, Children’s Hospital of Eastern Ontario, Ottawa, ON, Canada Marcella Aquino Rhode Island Hospital/Hasbro Children’s Hospital, Warren Alpert Medical School of Brown University, Providence, RI, USA Erin Banta NYU Winthrop Hospital, Division of Rheumatology, Allergy & Immunology, Mineola, NY, USA Anne K. Ellis Queen’s University, Kingston, ON, Canada Stanley Fineman Emory University School of Medicine, Atlanta Allergy & Asthma, Vienna, VA, USA Shannon French, MD, FRCPC McMaster University, Hamilton, ON, Canada Catherine Hammond Department of Pediatrics, Allergy/Immunology, University of Tennessee Health Science Center, Memphis, TN, USA Jay Lieberman Department of Pediatrics, Allergy/Immunology, University of Tennessee Health Science Center, Memphis, TN, USA Nicole B. Ramsey Department of Pediatrics, Division of Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, NY, USA David R. Stukus Division of Allergy & Immunology, Nationwide Children’s Hospital and The Ohio State College of Medicine, Columbus, OH, USA Julia E. M. Upton Division of Immunology and Allergy, Hospital for Sick Children, Toronto, ON, Canada Department of Paediatrics, University of Toronto, Toronto, ON, Canada Julie Wang Department of Pediatrics, Division of Allergy and Immunology, Icahn School of Medicine at Mount Sinai, New York, NY, USA Tonya Winders Allergy & Asthma Network, Global Allergy & Airways Patient Platform, Vienna, VA, USA vii Introduction to Anaphylaxis Essentials 1 Shannon French, Anne K. Ellis Introduction Anaphylaxis is a life-threatening severe systemic allergic reaction. It is caused by the rapid release of mast cell mediators into systemic circulation. It is most com- monly triggered by foods, insect stings, medications, and latex. It is typically a clinical diagnosis with an acute onset. Anaphylaxis was initially described in medi- cal literature in 1902 during a study which involved immunizing canines with jel- lyfish toxin. These injections resulted in a systemic allergic reaction in certain animals, rather than protection from their vaccine. This resulted in the term “ana- phylaxis,” which is derived from the Greek words “ana” (against) and “phylaxis” (protection) [1]. Anaphylaxis requires urgent recognition and treatment. Intramuscular epinephrine is the mainstay of treatment and should be administered as early as possible, with secondary measures to include H1 and H2 antihistamines, corticosteroids, IV fluids, oxygen, and bronchodilators. A period of observation is required following treatment. Atopic individuals are at a higher risk of developing anaphylaxis, such as those with asthma. Signs and Symptoms The presentation of anaphylaxis can be extremely variable. Symptoms generally start within 30 minutes of exposure to the triggering allergen, but may occasionally be more delayed. Early symptoms can be mild; however, they may quickly progress to a severe reaction. The signs and symptoms of anaphylaxis typically follow a uni- phasic course; however, biphasic reactions do occur. Biphasic reactions have been S. French McMaster University, Hamilton, ON, Canada A. K. Ellis (*) Queen’s University, Kingston, ON, Canada e-mail: [email protected] © Springer Nature Switzerland AG 2020 1 A. K. Ellis (ed.), Anaphylaxis, https://doi.org/10.1007/978-3-030-43205-8_1 2 S. French and A. K. Ellis Table 1.1 Signs and symptoms of anaphylaxis Cutaneous/subcutaneous/mucosal tissue Flushing, pruritus, urticaria, swelling, morbilliform rash, pilor erection Periorbital pruritus, erythema and swelling, conjunctival erythema, tearing Pruritus and swelling of the lips, tongue, uvula/palate Pruritus in the external auditory canals Pruritus of the genitalia, palms, soles Respiratory Nose: pruritus, congestion, rhinorrhea, sneezing Larynx: pruritus and tightness in the throat, dysphonia and hoarseness, dry staccato cough, stridor, dysphagia Lung: shortness of breath, chest tightness, deep cough, wheezing/bronchospasm Cyanosis Gastrointestinal Nausea, cramping abdominal pain, vomiting, diarrhea Cardiovascular Chest pain, palpitations, tachycardia, bradycardia, or other dysrhythmia Feeling faint, altered mental status, hypotension, loss of sphincter control, shock, cardiac arrest CNS Aura of impending doom (“angor animi,” uneasiness, throbbing headache, dizziness, confusion, tunnel vision; in infants and children, sudden behavioral changes, such as irritability, cessation of play, and clinging to parent) Other Metallic taste in the mouth Dysphagia Uterine contractions in post-pubertal female patients Adapted from Ref. [2] described to occur in approximately 4.6% of all anaphylactic events, based on a recent 2015 systematic review and meta-analysis [2]. Cutaneous findings are the most common symptoms in anaphylaxis, occurring in 80–90% of all episodes [3]. Signs and symptoms of anaphylaxis are listed in Table 1.1. Diagnostic Criteria Anaphylaxis is predominately a clinical diagnosis. Criteria for defining anaphylaxis were developed in 2004 by a panel of experts at the National Institutes of Health, which resulted in the publication of the NIAID/Anaphylaxis Network Definition of Anaphylaxis. The determined criteria for anaphylaxis are listed in Table 1.2 [4]. A study by Campbell et al. was done in 2012 to validate the criteria provided by the NIAID meeting. This study provided a sensitivity of 97%, specificity of 83%, nega- tive predictive value of 98%, and positive predictive value of 69% for these criteria [5]. Epidemiology The incidence and prevalence of anaphylaxis vary worldwide, with differences depen- dent on a number of variables. Anaphylaxis is likely underreported as well [6]. A 2006 report on anaphylaxis in the USA from the American College of Allergy Asthma and 1 Introduction to Anaphylaxis Essentials 3 Table 1.2 Clinical criteria for diagnosing anaphylaxis 1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal tissue, or both (e.g., generalized hives, pruritus or flushing, or swollen lips-tongue-uvula) and at least one of the following: (a) Respiratory compromise (e.g., dyspnea, wheeze-bronchospasm, stridor, reduced PEF, or hypoxemia) (b) Reduced BP or associated symptoms of end-organ dysfunction (e.g., hypotonia [collapse], syncope, or incontinence) 2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours): (a) Involvement of the skin-mucosal tissue (e.g., generalized hives, itch-flush, or swollen lips-tongue-uvula) (b) Respiratory compromise (e.g., dyspnea, wheeze-bronchospasm, stridor, reduced PEF, or hypoxemia) (c) Reduced BP or associated symptoms of end-organ dysfunction (e.g., hypotonia [collapse], syncope, or incontinence) (d) Persistent gastrointestinal symptoms (e.g., crampy abdominal pain or vomiting) 3. Reduced BP after exposure to a known allergen for that patient (minutes to hours): (a) Infants and children: low systolic BP (age specific) or greater than 30% decrease in systolic BP Simons et al. [3] Immunology (ACAAI) anaphylaxis workgroup quoted a lifetime prevalence between 0.05% and 2% [7]. In the 2006 NAIAD report, the incidence of anaphylaxis was reported to be approximately 10–20/100,000 population per year [8]. However, a 2013 European systematic review on the epidemiology of anaphylaxis reported inci- dence rates for all-cause anaphylaxis between 1.5 and 7.9 per 100,000 person-years. This review estimated that 0.3% (95% CI 0.1–0.5) of the population experience ana- phylaxis at some point over the course of their lives [9]. It has been described in the literature that anaphylaxis is becoming more frequent, with a study by Rudders et al. citing a 58% rise between 2000 and 2009 in the USA [10]. Pathophysiology Reactions which are described as “anaphylaxis” are classically thought of as being immunoglobulin-E (IgE) mediated, with non-IgE-mediated reactions being dubbed “anaphylactoid.” Clinically, these two types of reaction are identical. It has been proposed by the World Allergy Organization (WAO) that the term anaphylactoid be discarded. Instead, the WAO has proposed that anaphylactic reactions be catego- rized as immunologic and non-immunologic. Immunologic anaphylaxis is typically described as IgE mediated, with non-immunologic anaphylaxis being a result of sudden basophil or mast cell degranulation in the absence of immunoglobulins [11]. The traditional IgE-mediated mechanism of anaphylaxis begins with an antigen binding to an allergen-specific IgE. Antigen-bound IgE in turn binds to the receptor Fc-epsilon-RI on mast cells and/or basophils. This causes these cells to degranulate, releasing a number of inflammatory mediators. These inflammatory mediators include histamine, tryptase, heparin, chymase, cytokines (i.e., tumor necrosis factor, 4 S. French and A. K. Ellis IL-4, IL-13), prostaglandin D2, leukotriene B4, platelet-activating factor (PAF), and the cysteinyl leukotrienes LTC4, LTD4, and LTE4. Histamine and tryptase are two of the most abundant preformed granule mediators released by mast cells and baso- phils during episodes of anaphylaxis. Release of these mediators causes the symp- toms which are seen in anaphylaxis, such as vasodilation, angioedema, bronchial smooth muscle contraction, urticaria, and pruritus [12, 13]. Differential Diagnosis The differential diagnosis for anaphylaxis is broad and is age dependent to some degree. Table 1.3 includes a number of entities which can mimic anaphylaxis [2]. Table 1.3 Differential diagnosis of anaphylaxis Common disorders Acute generalized urticaria and/or angioedema Acute asthma Vasovagal syncope (faint) Panic attack/acute anxiety attack Aspiration of a foreign body Cardiovascular events (myocardial infarction, pulmonary embolus) Neurologic events (e.g., seizure, cerebrovascular event [stroke]) Shock Hypovolemic Cardiogenic Distributive (e.g., sepsis, spinal cord injury) Obstructive (e.g., pulmonary embolism, tension pneumothorax, cardiac tamponade) Excess endogenous histamine Mastocytosis/clonal mast cell disorders Basophilic leukemia Flush syndromes Perimenopause Carcinoid syndrome Autonomic epilepsy Medullary carcinoma of the thyroid Postprandial syndromes Scombroidosis Anisakiasis Pollen-food allergy syndrome Food poisoning Caustic ingestion (children) Other nonorganic disease Vocal cord dysfunction Hyperventilation Psychosomatic episode Other Nonallergic angioedema (hereditary angioedema, angiotensin-converting enzyme inhibitor- associated angioedema) Systemic capillary leak syndrome Red man syndrome (vancomycin) Pheochromocytoma (paradoxical response)
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